Frontal Fibrosing Alopecia: A Review of Disease Pathogenesis

Frontal fibrosing alopecia (FFA) is a type of irreversible hair loss, often seen in postmenopausal women, characterized by a receding frontal and temporoparietal hairline. The pathogenesis of FFA is complex and not fully understood, but it is believed to involve immune cell and substance-mediated inflammatory responses, with histological findings showing inflammatory cell infiltration around lesioned hair follicles. The disease is associated with a collapse of immune privilege in hair follicles and is linked to many autoimmune diseases. Factors such as interferon-γ (IFN-γ), epithelial-mesenchymal transition (EMT), peroxisome proliferator-activated receptor γ (PPAR-γ), and the mammalian target of rapamycin (mTOR) signaling pathway play a role in the disease's progression. Genome-wide association analysis indicates that FFA is an immune inflammatory disease with a genetic predisposition, specifically driven by HLA-B*07:02. The roles of sex steroids and external stimuli in FFA are speculative and derived from clinical studies of disease behavior. More extensive studies are needed to confirm the actual pathogenesis of FFA.